Cardiac rhythm management devices are implantable devices that provide electrical stimulation to selected chambers of the heart in order to treat disorders of cardiac rhythm and include pacemakers and implantable cardioverter/defibrillators. A pacemaker is a cardiac rhythm management device that paces the heart with timed pacing pulses. (As the term is used herein, a pacemaker is any cardiac rhythm management device with a pacing functionality, regardless of any other functions it may perform such as delivery of cardioversion/defibrillation shocks.) The most common condition for which pacemakers are used is in the treatment of bradycardia, where the ventricular rate is too slow. Atrio-ventricular conduction defects (i.e., AV block) that are permanent or intermittent and sick sinus syndrome represent the most common causes of bradycardia for which permanent pacing may be indicated. If functioning properly, the pacemaker makes up for the heart's inability to pace itself at an appropriate rhythm in order to meet metabolic demand by enforcing a minimum heart rate. Pacing therapy may also be applied in order to treat cardiac rhythms that are too fast, termed anti-tachycardia pacing.
Also included within the concept of cardiac rhythm is the manner and degree to which the heart chambers contract during a cardiac cycle to result in the efficient pumping of blood. For example, the heart pumps more effectively when the chambers contract in a coordinated manner. The heart has specialized conduction pathways in both the atria and the ventricles that enable the rapid conduction of excitation (i.e., depolarization) throughout the myocardium. These pathways conduct excitatory impulses from the sino-atrial node to the atrial myocardium, to the atrio-ventricular node, and thence to the ventricular myocardium to result in a coordinated contraction of both atria and both ventricles. This both synchronizes the contractions of the muscle fibers of each chamber and synchronizes the contraction of each atrium or ventricle with the contralateral atrium or ventricle. Without the synchronization afforded by the normally functioning specialized conduction pathways, the heart's pumping efficiency is greatly diminished. Patients who exhibit pathology of these conduction pathways, such as bundle branch blocks, can thus suffer compromised cardiac output. Heart failure (HF) refers to a clinical syndrome in which an abnormality of cardiac function causes a below normal cardiac output that can fall below a level adequate to meet the metabolic demand of peripheral tissues. Heart failure can be due to a variety of etiologies with ischemic heart disease being the most common (e.g., HF resulting from a myocardial infarction or MI). Intraventricular and/or interventricular conduction defects are commonly found in HF patients. In order to treat these problems, cardiac rhythm management devices have been developed which provide electrical pacing stimulation to one or more heart chambers in an attempt to improve the coordination of atrial and/or ventricular contractions, termed cardiac resynchronization therapy (CRT). Currently, a most common form of CRT is biventricular pacing in which paces are delivered to both ventricles in a manner that synchronizes their contractions.
Bradycardia pacing and CRT are delivered using bradycardia pacing modes that determine how the pacing pulses are delivered in response to sensed cardiac events and lapsed time intervals. Such modes may either be single-chamber pacing, where either an atrium or a ventricle is paced, or dual-chamber pacing in which both an atrium and a ventricle are paced. Particular modes may be designated by a letter code of three positions where each letter in the code refers to a specific function of the pacemaker. The first letter refers to which heart chambers are paced and which may be an A (for atrium), a V (for ventricle), D (for both chambers), or O (for none). (As the code is used herein, when an atrium or ventricle designated as paced, this may also refer to multiple site pacing such as biatrial or biventricular pacing.) The second letter refers to which chambers are sensed by the pacemaker's sensing channels and uses the same letter designations as used for pacing. The third letter refers to the pacemaker's response to a sensed P wave from the atrium or an R wave from the ventricle and may be an I (for inhibited), T (for triggered), D (for dual in which both triggering and inhibition are used), and O (for no response). Additional sensing of physiological data allows some pacemakers to change the rate at which they pace the heart in accordance with some parameter correlated to metabolic demand. Such pacing is called rate-adaptive pacing and is designated by a fourth letter added to the three-letter code, R. Modern pacemakers are typically programmable so that they can operate in any mode which the physical configuration of the device will allow.
Pacemakers can enforce a minimum heart rate either asynchronously or synchronously. In asynchronous pacing, the heart is paced at a fixed rate irrespective of intrinsic cardiac activity. There is thus a risk with asynchronous pacing that a pacing pulse will be delivered coincident with an intrinsic beat and during the heart's vulnerable period which may cause fibrillation. Most pacemakers for treating bradycardia or delivering CRT today are therefore programmed to operate synchronously in a so-called demand mode where sensed cardiac events occurring within a defined interval either trigger or inhibit a pacing pulse. Inhibited demand pacing modes utilize escape intervals to control pacing in accordance with sensed intrinsic activity. In an inhibited demand mode, a pacing pulse is delivered to a heart chamber during a cardiac cycle only after expiration of a defined escape interval during which no intrinsic beat by the chamber is detected. If an intrinsic beat occurs during this interval, the heart is thus allowed to “escape” from pacing by the pacemaker. Such an escape interval can be defined for each paced chamber. For example, a ventricular escape interval can be defined between ventricular events so as to be restarted with each ventricular sense or pace. The inverse of this escape interval is the minimum rate at which the pacemaker will allow the ventricles to beat, sometimes referred to as the lower rate limit (LRL).
During normal physiological beats, atrial contractions augment the diastolic filling of the ventricles. When the ventricles are paced upon expiration of a ventricular escape without regard to atrial activity such as in a VVI mode, the normal synchrony between atrial and ventricular contractions that occurs in intrinsic physiological beats is lost. Such atrio-ventricular dyssynchrony can compromise cardiac output to a clinically significant extent, sometimes referred to as pacemaker syndrome. It is therefore normally preferable to employ atrial triggered pacing modes that attempt to maintain the physiological synchrony between atrial and ventricular contractions.
In atrial triggered modes (e.g., VDD and DDD modes), another ventricular escape interval is defined between atrial and ventricular events, referred to as the atrio-ventricular delay interval or AVD. The atrio-ventricular interval is triggered by an atrial sense or pace and stopped by a ventricular sense or pace. A ventricular pacing pulse is delivered upon expiration of the atrio-ventricular interval if no ventricular sense occurs before. The value of the atrio-ventricular interval for optimal preloading of the ventricles will vary with heart rate and in a manner that differs from patient to patient. If a patient has a physiologically normal atrial rhythm, ventricular pacing triggered by atrial senses also allows the ventricular pacing rate to be responsive to the metabolic needs of the body. If the atrial rhythm is too slow, the device can be configured to pace the atria on an inhibited demand basis such as in DDD mode which may include rate-adaptive pacing. An atrial escape interval is then defined as the maximum time interval in which an atrial sense must be detected after a ventricular sense or stimulus before an atrial stimulus will be delivered. The lower rate limit interval is then the sum of the atrial escape interval and the atrio-ventricular interval.
In a patient with normal AV conduction (i.e., no degree of AV block) and normal ventricular function, the optimum AVD that maximizes cardiac output will usually correspond closely with the intrinsic atrio-ventricular interval. When such an AVD is used for bradycardia pacing of the ventricles, the ventricular pace is thus delivered close to the time that the ventricles become excited due to intrinsic AV conduction. Similarly, an optimum AVD for resynchronizing the ventricles with biventricular pacing in a patient with intact AV conduction will usually involve pre-exciting the ventricle having the conduction deficit with an AVD that causes that ventricle to contract at roughly the same time that the contralateral ventricle contracts due to intrinsic AV conduction. As described below, however, in patients with compromised ventricular function, it may be advantageous at times to employ an AVD for ventricular pacing that is much shorter than the intrinsic atrio-ventricular interval.